Implantable medical interventional device with shifting zones of tachycardia recognition and therapy

ABSTRACT

A device-implemented method detects and treats abnormal (i.e., pathologic) tachycardias experienced by a patient with an implanted automatic defibrillator. The defibrillator has the capability to distinguish pathologic tachycardia from physiologic tachycardia by the application of predetermined distinction criteria programmed into it. Changes in a physiologic parameter of the patient which signify a physiologic basis for increase or decrease of the patient&#39;s heart rate are detected, and in response, the distinction criteria are modified to enhance the capability of the defibrillator to make the distinction between pathologic and physiologic tachycardia when this change in circumstances that would otherwise tend to obscure the distinction is factored in. In one method, the parameter under detection is patient activity, and the distinction criteria include a threshold heart rate above which the patient is presumed to be experiencing a pathologic tachycardia. The threshold rate is shifted up or down depending on whether the detected change is indicative of an increase or a decrease, respectively, of the patient&#39;s heart rate.

CROSS-REFERENCE TO RELATED APPLICATION

This application is a division of U.S. patent application Ser. No.07/916,588, filed Jul. 20, 1992, now U.S. Pat. No. 5,370,667 which is acontinuation-in-part of application Ser. No. 07/863,092 filed Apr. 3,1992, now U.S. Pat. No. 5,342,404, dated Aug. 30, 1994.

BACKGROUND OF THE INVENTION

The present invention relates generally to implantable medical devices,and more particularly to an implantable interventional device such as anantitachycardia pacemaker, a cardioverter, a defibrillator, or a devicehaving a combination of such functions, adapted to deliver electric in,pulse or shock therapies to the patient's heart upon detection of aventricular tachycardia (VT) or ventricular fibrillation (VF). Moreparticularly, the invention relates to improvements in apparatus andmethods for detecting and distinguishing pathological tachycardias fromphysiological tachycardias and for establishing the type and timing ofthe delivery of the appropriate therapy upon detection of pathologic VTor VF.

Sinus heart rates in normal healthy adults may range upward to 160 beatsper minute (bpm) during physical activity or exercise, or even when theindividual is experiencing emotional stress or excitement. Rates up toeven 200 bpm may be experienced during strenuous exercise. Such elevatedrates occurring in these circumstances are a normal reaction by theorganism and are termed physiological tachycardias. The heart rategradually, perhaps even quickly, decreases to the normal resting ratewhen the factors leading to the increased rate have ceased.

In contrast, random or spontaneous elevation of the heart rate to suchlevels for no apparent reason constitutes pathological tachycardiaattributable to cardiovascular disease, and requires intervention withappropriate medical therapy. In general, pathological tachycardia in theatrium is tolerated because the excitable A-V junction tissue (betweenthe atrium and ventricle) has a longer refractory period and slowerconductivity than myocardial tissue, so that the rapid atrialcontractions typically fail to induce correspondingly rapid ventricularcontractions, allowing cardiac output to remain relatively strong with aventricular rhythm nearer the sinus rate.

On the other hand, pathological tachycardia in the ventricles, the mainpumping chambers of the heart, is not well tolerated. The rapidcontractions permit only partial filling of the chambers with oxygenatedblood and result in diminished cardiac output. Moreover, ventriculartachycardia (VT) tends to accelerate spontaneously to ventricularfibrillation (VF), in which synchronous contractions of the tissue ceaseand the myocardial contractions become random and uncoordinated. Theresulting loss of cardiac output requires immediate intervention todefibrillate, failing which death will ensue. Generally, VF occurs onlyafter VT; only rarely is VF not precipitated by a pathologicaltachycardia.

Although atrial tachycardia (AT) is relatively common, patients who aresymptomatic or at high risk may be treated with drugs, antitachycardiapacemakers, or in some extreme cases, such as where the AT tends toescalate to atrial fibrillation (AF), by performing a surgical A-V blockand a ventricular pacemaker implant. Antitachycardia pacemakers, whichoften are also prescribed for patients suffering VT, are usually adaptedto overstimulate the heart by applying pulses at a programmed rapid rateto suppress the ectopic activity that leads to premature atrial orventricular contractions. Pulses of relatively low energy content maysuffice to break the tachycardia and restore normal heart rate. The term"cardioversion" usually implies delivery of higher energy electricalshocks to the heart to break the tachycardia. Unfortunately, bothantitachycardia and cardioversion therapies which are used forterminating VT can contribute to acceleration into VF.

Defibrillators are employed to apply one or more high energy electricalshocks to the heart in an effort to overwhelm the uncoordinatedcontractions of the various sections of the myocardial tissue andreestablish organized spreading of action potentials from cell to cell,thereby to restore synchronized contractions of the ventricles.Automatic implantable defibrillators were described in the literature atleast as early as 1970, in separate articles of M. Mirowski et al. andJ. Schuder et al. Innovations since proposed have included automaticimplantable defibrillators which perform multiple functions ofantitachycardia, cardioversion and defibrillation, and whereappropriate, demand bradycardia pacing. In general, the desire is to useone or more pulse sequence or low level shock therapies for breaking VTbefore it spontaneously progresses into VF, and, if that fails or if VFoccurs without preliminary pathologic tachycardia, to resort to a highenergy defibrillating shock.

Typically, the shocks are delivered from one or more output storagecapacitors of sufficient capacity in the implanted device. Energyrequirements generally range from as little as 0.05 joule to up to 10joules for cardioversion, and from 5 joules to about 40 joules fordefibrillation, depending on the patient, the nature of the electricalwaveform applied, and the efficiency of the energy transfer through theelectrodes and into the heart tissue. The capacitors must be charged tothe level appropriate for the therapy when the dysfunction ordysrhythmia is detected, so that the energy required for the shock willbe rapidly available for delivery. Multiphasic shocks have been foundquite effective. It is customary to provide a preset delay betweensuccessive shocks, and to inhibit further shocks when return to normalrhythm is detected.

As used in this specification, the terminology "shock" or "shocks" mayinclude any pulse-type waveform, whether single phase or multiphase,which is delivered as antitachycardia, cardioverting or defibrillatingtherapy to a patient's heart in an effort to break, interrupt orterminate pathologic tachycardia or fibrillation and return the pumpingaction of the heart to a rate in the normal range; and "interventionaldevice" includes any antitachycardia pacemaker, cardioverter,defibrillator or other device or combination thereof (which may includethe function of conventional bradycardia pacing) which is adapted to beimplanted or otherwise worn by a human or animal subject for the purposeof intervening to deliver shocks to the heart in response to detectionof an abnormally rapid heart rate. The waveform is not limited to anyparticular energy content or range of energy content, and indeed, thetherapy may include burst stimulation or other conventional techniquesfor applying stimulation pulses (such as for rapid pacing) to break aVT.

Proper operation of implantable antitachycardia pacemakers,cardioverters, defibrillators and similar medical devices necessitatesproper timing of delivery of the therapy, including timing of chargingand firing of shock-producing output capacitors. It is essential, first,that the device have the capability to distinguish physiologicaltachycardias from pathological tachycardias to assure that occurrence ofthe former will not be wrongly identified as the latter with the resultthat the patient is subjected to a shock when he or she is merelyexercising, for example. Incapability to distinguish can mean, at thevery least, that the capacitors are needlessly charged, and worse, thatthey are inappropriately discharged into the heart, with consequencesranging from painful shock and possible loss of consciousness torepetitive shocks.

In copending U.S. patent application Ser. No. 07/863,092 filed Apr. 3,1992, ("the '092 application"), of which this application is acontinuation-in-part, and which is incorporated herein by reference,physiological and pathological tachycardias are distinguished by resortto the use of two independent sensors, one of which detectselectrocardiogram (ECG) or intrinsic electrical heart activity and theother, physical exercise by sensing activity. The latter sensor may betermed a complementary sensor, which, in the preferred embodiment of theinvention disclosed in that application, is an accelerometer fordetecting patient activity directly, but which instead might be anindirect sensor of physical exercise of the patient, such as bloodpressure, blood oxygen content, minute ventilation, central venoustemperature, pulse rate, or blood flow detector. Concurrent detection ofpatient cardiac activity (ECG) as well as physical activity providesimproved discrimination between physiologic and pathologic tachycardias,particularly in an overlap range of heart rates from about 130 to about180 beats per minute (bpm). This range presents especially seriousproblems when ECG detection alone is used and/or the patient may beexperiencing either a fast physiological tachycardia or a relativelyslow pathological VT.

For example, the ECG signal may indicate a VT of 150 bpm which is in therange of both pathologic and physiologic tachycardia for a particularpatient, but if the activity status sensor (e.g., accelerometer) detectsphysical activity, the device would be inhibited from deliveringantitachycardia treatment. On the other hand, the ECG may demonstrate VTor VF at a time when the activity status sensor indicates no movement ofthe patient, leading to the decision to trigger prompt therapy. Thedecision, therefore, is a reasoned one and is made automatically, and inthe case of origin of a tachycardia, discriminates between physiologicand non-physiologic.

An implantable medical interventional device utilizing the complementarysensors may be programmed to respond to sensing an ECG signal indicativeof possible slow VT, coupled with confirmation of physical inactivity ofthe patient by the other sensor, by stimulating the heart with lowenergy shocks to break the VT before it accelerates into VF.Alternatively, a more liberal programming philosophy may be followed inwhich slow tachycardia and lack of physical activity of the patientmerely define an alert condition of the device in which the capacitorsare charged to the proper energy level, in anticipation of thepossibility that a more dramatic situation may develop. If delivery ofan antitachycardia or defibrillating shock is subsequently determined tobe warranted, precious time will not have been lost waiting for theoutput storage capacitors of the device to be charged.

The use of two complementary sensors serves not only to control chargingand firing of the implantable interventional device for treatment oftachycardias and fibrillation, but to better evaluate the probability ofsuccess of interventional measures. Since VT may be broken by lowerenergy shocks than those needed to terminate VF, a considerable energysaving is achieved which helps to reduce the size of the battery and,consequently, of the implanted device itself, or to increase itslifetime with the same battery capacity, either of which is important tothe development of self-powered implanted devices.

Numerous conventional electrical waveform therapies or therapy protocolsmay be programmed into the interventional device for selectiveapplication to the heart upon detection of an applicable cardiac eventby the complementary sensors. For example, these may include singlestimulating pulses, stimulating pulse sequences, stimulating pulsetrains of variable repetition frequency, one or more bursts ofstimulating pulses, and single phase or multiple phase shocks ofvariable energy content generally greater than the energy content of thepulses in the other protocols which are utilized for treatment. Ingeneral, the therapy is applied in successively more stringent protocolsuntil it is successful to break the VT or VF. This is termed a "tiered"therapy.

Both the degree of difficulty to defibrillate and the likelihood offailure increase with the length of time that the patient is infibrillation. It is crucial to reduce the time interval from onset offibrillation to delivery of the initial shock to a minimum, to reducethe energy required to defibrillate the heart and to increase theopportunity to successfully resuscitate the patient. As pointed outabove, it is considerably easier to interrupt a VT, which may requiredelivery of only one joule of electrical energy, than to terminate VFwith the potential requirement of 15 joules or more in each shock.Correspondingly, resuscitation is much more achievable with a patientwho has been in fibrillation for only a few seconds than if the attackhas continued for several minutes. Prompt treatment is also importantfor the patient experiencing either VT or VF and fighting against lossof consciousness. An excessive interval from onset to delivery oftherapy, e.g., ten to thirty seconds, may cause the patient to faint,whereas earlier intervention might well have allowed the circulatorysystem to compensate for the fast heart rate without the loss ofconsciousness.

This type of dual sensing helps the implanted programmablemicroprocessor-based interventional device to better interpret anddistinguish tachycardias than the ECG criteria which typically has beenused in prior art devices, such as heart rate, morphology of the ECG,sudden onset, rate stability, etc. At least in pan this is because theactivity status sensor is complementary, providing additionalinformation concerning the cardiac event under scrutiny, rather thanmerely pan of the ECG criteria. As noted in the '092 application,improved discrimination is especially pronounced in the borderlineregion from 130 bpm to 180 bpm, thereby better avoiding needless,painful and debilitating shocking of the heart.

It is a principal object of the present invention to provideimprovements in techniques for recognizing abnormal tachycardias, overthe prior an and even that disclosed in the '092 application,particularly in the overlap or borderline region where pathologicaltachycardias had been virtually indistinguishable from physiologicaltachycardias.

SUMMARY OF THE INVENTION

The present invention, in one of its principal aspects, takes advantageof the detection capabilities of the complementary sensor, such as anaccelerometer, to modify the rate criterion which is used forpathological tachycardia recognition. If the accelerometer indicates thepatient is at rest, the criterion for deciding that a pathologicaltachycardia is in progress is set at a rate of 130 bpm, for example; onthe other hand, if the accelerometer indicates patient activity, thetachycardia rate criterion is shifted to 170 bpm.

This is vastly different from the technique used in the prior art. Theproblem that exists with the prior art devices is that they invariablyemploy a single fixed rate which represents a compromise between theheart rate the particular patient might exhibit during exercise and therate thought to be indicative a pathological tachycardia. The overlapmakes it very difficult to accurately determine whether the event ofinterest warrants intervention because some individuals may have apathological tachycardia rate of 140 bpm, or even 130 bpm, and yet mayalso exhibit an exercise tachycardia rate of 140 bpm, or even 150 bpm.If the prior art rate criterion for such a patient were set at 140, thepatient would receive a defibrillating shock from the implantedautomatic defibrillator when he or she is merely exercising.

Although currently available cardioverters/defibrillators are adapted tooperate on the principle of applying a whole bundle of distinct ECGcriteria to recognize a tachycardia (pathological), including suddenrate change, rate stability, probability density function, and so forth,the principal criterion used is purely rate. If any rate above 160 bpmis considered to be pathological, these devices can fail to recognize atachycardia for which intervention is needed where the rate in questionis anywhere below 160 bpm.

With the present invention, the intervention rate is easily adjusted orshifted according to the status of patient activity or exercise, whichis to say, the rate criterion for tachycardia recognition applied to theECG signal is changed simply and effectively depending upon the outputor merely the status of the complementary sensor.

The present invention modifies the criteria to recognize a pathologictachycardia by assessing the ECG signal according to the output signalof the activity status sensor. That is, if the output signal of theactivity status sensor is not present or is quite low, indicative ofrest, the pathologic tachycardia recognition ECG rate criterion ispreprogrammed to be correspondingly low (e.g., perhaps a heart rate of130 bpm); but when the activity sensor output increases, indicative thatthe patient is undergoing exercise, the rate criterion is programmed toshift automatically to a higher value (increasing to, perhaps, 150 oreven 170 bpm, depending on the particular patient). In the preferredembodiment, this threshold rate moves up or down according to the statusof the output signal of the accelerometer. This provides information notonly about the pathological tachycardia rate but also its morphology.

As in the device of the '092 application, the implantable medicalinterventional device of the present invention responds to detection ofcardiac activity of the patient indicative of the abnormal VT or of VFby selectively applying to the patient's heart a conventionally selectedsequence of different electrical waveforms (e.g., single pulse, dualpulses, pulse trains or bursts, biphasic or triphasic shocks, etc.).Each time a new waveform is applied or repeated during the course oftreatment of an ongoing VT or VF, the ECG is monitored to determinewhether that treatment was successful, and, if not, the therapy iscontinued. Otherwise, it is terminated. A control means which is afunction of the microprocessor software, or an independent subsystem ofthe overall electronics system package of the device, selects theappropriate electrical therapy for the sensed abnormal tachyrhythmiaaccording to the programmed response to the recognized event. The devicefurther includes an evaluation means operatively associated with thecontrol means for modifying or adjusting the ECG criteria, andspecifically the tachycardia recognition rate or threshold rate by whichnormal tachycardias are discriminated from abnormal tachycardias,according to the status of the activity signal, i.e., whether itindicates inactivity or activity, and in the latter case, the generalextent or level of the activity.

The threshold rate is shifted to higher values with commencement orincreases of physical activity by the patient and shifted to lowervalues with decreases or cessation of the physical activity. Theelectrical therapy may be tiered so that the shift applies to entiredifferent zones of ECG recognition rates and to the related therapeuticconsequences of a tachycardia recognized in one of the zones, such asincreasingly aggressive therapy protocols applied with eithercontinuation or acceleration of the tachycardia and the initial therapyselected for a protocol.

Therefore, it is another object of the invention to provide a simple andeffective technique for identifying tachycardias arising from heart orcardiovascular disease, for distinguishing them from naturally occurringelevated heart rates attributable to stress including physical exerciseby the application of an ECG rate criterion which is controlled by anon-ECG sensor output, and for shifting the ECG rate criterion inresponse to a material change in the non-ECG sensor output.

According to another significant aspect of the present invention, anatrial bipolar electrode is used to check the status of the atrial ECGto detect atrial tachycardia. The purpose is to avoid one of theproblems associated with conventional implantable defibrillators, viz.,that of inappropriate firing (i.e., discharge of the capacitors todeliver the shock(s) to the heart). This may occur, for example, wherethe tachycardia recognition criteria is set within a zone encompassing aventricular rate such as 130 to 140 bpm, and the patient experiencesatrial fibrillation with that ventricular rate. The complementaryactivity sensor used in the apparatus of the invention may not beentirely helpful in these circumstances, because it could be indicatingat that time that the patient is resting or undergoing mild activity, ifthat is the case, with a consequent lowered tachycardia recognitionrate. Hence, if the status of the atrial ECG were not being detected,the patient would receive a shock in the region of the ventricles. Byuse of an atrial bipolar electrode for such sensing, the device of theinvention avoids the delivery of such a shock.

According to another, associated feature of the invention, detection ofatrial fibrillation in this way is used to trigger the delivery of lowenergy shocks such as in the energy range from 0.25 to 1.0 joule fromthe implanted device to the atrial chambers, and thereby defibrillatethe atrium alone. A tiered therapy regimen may be used here as well, toprovide an improved protocol for treating atrial dysrhythmias such asatrial flutter, atrial tachycardia or atrial fibrillation.

Therefore, yet another object of the invention is to avoid inappropriatefiring of the implanted defibrillator into the ventricles when thepatient is actually experiencing atrial fibrillation, by detecting thestatus of the atrial ECG.

A further object of the invention is to defibrillate the atrium aloneupon such detection of atrial fibrillation, and to employ a tieredtherapy regimen to treat atrial dysrhythmias.

According to still another aspect of the invention, the R-Rinterval--the coupling interval between beats--is detected and theventricular ECG signals are analyzed to determine whether thetachycardia is regular or a variation in the R-R intervals. A variationin the R-R coupling interval is an indication that atrial dysrhythmia isoccurring. It is desirable in such a situation to seek to terminate theatrial dysrhythmia, which will eliminate the VT because the atrialproblem is primary and the VT is only secondary--rather than to attemptto terminate the VT directly. It follows that in this case it would beundesirable to modify the tachycardia recognition rate. Suchmodification is used specifically for detection of VT under conditionsindicative of apparent exercise by the patient, which clearly is notoccurring in this case. Accordingly, the modification response to theactivity sensor output is disabled when a variation in the R-R intervalis detected while a VT is occurring.

Hence, it is still another object of the present invention to determinewhether a detected VT is primary or secondary by observing the nature ofthe R-R interval, and specifically to direct the implantedcardioverter/defibrillator to apply a therapy to terminate atrialdysrhythmia rather than to apply a therapy directly toward breaking theventricular tachycardia.

A further object of the invention is to disable the VT recognitioncriteria modification-producing circuitry of the tachycardia detector ofan implantable defibrillator when atrial dysrhythmia is occurring, byperforming the disabling function when a varying R-R interval, incontrast to a regular R-R interval, is detected in the patient's ECG.

BRIEF DESCRIPTION OF THE DRAWINGS

The above and other objects, aspects, features and attendant advantagesof the present invention will become apparent from a consideration ofthe following detailed description of a presently preferred embodimentand method, taken in conjunction with the accompanying drawings, inwhich:

FIG. 1 is a graph illustrating readouts measured in g versus time from anon-ECG sensor implanted in a patient;

FIG. 2 is a perspective view of a non-ECG sensor in the form of anactivity status sensor (accelerometer) comprised of a pair of mercuryball sensors in fixed orthogonal orientation as implanted in a patient;

FIGS. 3 is another embodiment of an accelerometer, fabricated in anintegrated or hybrid electronic circuit;

FIG. 4 is a simplified diagram of an implantable medical interventionaldevice with activity status sensor(s) located within the device housing;

FIG. 5 is a graph of heart rate versus time relative to intervals ofpatient rest and exercise, illustrating the concepts of the presentinvention for shifting the ECG tachycardia recognition rate or entirezone of rates up or down under the control of the non-ECG sensor output;

FIG. 6 is a phantom view of a patient having an implanted medicalinterventional device adapted to provide such threshold rate or zoneshifting according to the invention, together with an implantedmulti-electrode lead;

FIG. 7 is a block diagram of circuitry used for evaluation of a selectedportion of the electrical cardiac activity of the patient according toanother aspect of the invention; and

FIG. 8 is an alternative embodiment to that of FIG. 4, in which thesensor is housed in its own separate case and connected by an electricallead to a connector on the device housing.

DESCRIPTION OF THE PREFERRED EMBODIMENT AND METHOD

The implantable medical interventional device to be described utilizes adirect sensor of electrical cardiac activity such as an ECG sensor, andan activity status sensor adapted to detect the position and movementsof the patient, in the form of an accelerometer or otherelectromechanical converter, which may be calibrated for both static anddynamic outputs. The static output will depend upon the physicalposition or posture of the implant patient when inactive (e.g., at rest,or in a state of collapse). Assume that the activity status sensor isoriented vertically when implanted, and in that position produces a zerog (i.e., unit of gravity) output. The sensor produces a +1 g output inone aspect of its horizontal orientation, (i.e., one major side down),and produces a -1 g output in the opposite aspect of horizontalorientation (the other major side down).

In the example of FIG. 1, the activity status sensor provides a zeroreading when the patient is standing during a first time interval, a +1when the patient is supine during a second time interval, and a -1 whenthe patient is prone during a third interval. This chart is not intendedto show the response of the activity status sensor to changes inposition, such as in the period between the first and second intervals,but only that different readouts or signals are produced by the sensorupon detection of different static positions of the patient.

The particular outputs may be modified by calibrating the sensor forslight deviations of orientation relative to these three positions. Ifthe patient were lying on a side, the sensor reading would not be +1 or-1, but a non-zero value. By calibrating the electrical output of thesensor circuit after implantation, or by autocalibration of the deviceitself, the orientation of the sensor in any position of the patientwill be known from the readout. By employing a second such activitystatus sensor with a 90° orientation relative to the first sensor, eachsensor recognizes two of the three mutually orthogonal axes (X-Y-Z) inthree dimensional space, and both together detect a full three axisorientation, to provide a combined reading uniquely identifying thepatient's position. Thus, the sensor may be used to detect static orstable (i.e., non-moving) position of the patient, and patient activityconstituting dynamic movements of the patient, such as a momentarychange of position or continuing movements such as walking, dancing,bicycling, and so forth.

The activity status sensor may be of the mercury ball type described inU.S. Pat. No. 4,846,195. If a single such sensor were used as an X-Yaxes (two dimensional) detector, it would not uniquely identify patientposition. Two such sensors with fixed orthogonal orientation willprovide combined detection of all three axes (X-Y-Z) of position ordirection of movement. Referring to FIG. 2, sensor 10 includes a pair ofmercury ball sensors 12 and 13 coupled together at an angle of 90degrees. This fixed orientation of the two assures that their combinedoutput signal will properly identify different specific physicalpositions of the patient even if the overall sensor were to undergo ashift in its orientation after implantation in the patient's body.

It is desirable that the orientation of the sensors after implantationbe such that one of them (sensor 13, in this example) is approximatelyhorizontal and the other (here, sensor 12) approximately vertical whenthe patient is standing upright. In the exemplary configurationrepresented in FIG. 2, sensor 12 is somewhat smaller than and assembledwithin sensor 13 in the fixed relationship. In practice, the twoposition sensors may be separated, but nevertheless fixed in theirorthogonal orientation. Under static (motionless) conditions of eithersensor of the pair, the mercury ball (not shown) is at rest and contactsspecific ones among the set of electrodes (electrical contacts) 14disposed about the side or floor of the sensor chamber. The electrodesare connected by respective electrical conductors to the output circuitof the sensor, each set of electrode locations in conductive contactidentifying a particular position of the patient. As the patient changesposition or engages in ongoing physical activity, one or both mercuryballs will roll about within their respective chambers and make andbreak contact with the electrodes. The combined static locations of themercury balls within the sensor pair, or their dynamic locations as theymake and break connections between adjacent electrodes (closures andopenings with time) is detected to provide information regarding thephysical position, change in position, and ongoing movements of thepatient.

In an alternative embodiment, the accelerometer may be piezoelectric,piezoresistive or piezocapacitive, fabricated in silicon or othersemiconductor material within an integrated electronic or hybridcircuit, such as that described in U.S. Pat. No. 5,031,615. A hybridsemiconductor integrated circuit incorporates the accelerometer as amicrominiature mechanoelectrical converter or transducer of highefficiency and low power consumption. This type of accelerometer 15,shown in FIG. 3, has a silicon monocrystalline substrate 15-1, anepitaxial doped layer 15-2 overlying the surface of substrate 15-1, anda polycrystalline silicon layer 15-3 sandwiched between passivatinglayers 15-4, 15-5 of silicon dioxide. A cavity 15-6 is formed in thesubstrate by etching, and portions of the silicon and passivating layersare removed by micromachining, forming a rectangular plate 15-7connected by four arms to the comers of the cavity. The plate and itsarms constitute the acceleration responsive element. An additional upperlayer may be provided with an opening contiguous with the cavity toallow axial movement of plate 15-7 on its arms, and a protective layerof glass then disposed over the structure. An integrated circuitsuitable for processing the movements of the plate in response toacceleration to provide the activity status signal may be fabricated inthe silicon substrate, within the region generally below that designatedby 15-8, by conventional semiconductor processing techniques.

FIG. 4 is a simplified diagram of an implantable medical interventionaldevice such as a defibrillator 25 adapted to provide bothantitachycardia and defibrillation therapies. The defibrillator includesbatteries 27, electronics 29 (e.g., including a microprocessor 29-1,signal processing circuitry 29-2, sense amplifiers 29-3, memories 29-4,and other conventional components) and output capacitors 30 for storingelectrical charge in variable quantities according to the amount ofelectrical energy to be delivered for shocking the heart to provide thedesired therapy. The activity sensor is located within the defibrillatorin the form, for example, of an accelerometer 34 with orthogonallyoriented mercury ball sensors 35, 36 substantially as described in thetext pertaining to FIG. 2, except that the two may be separately affixedto maintain that orientation. Accelerometer 34 is housed within butmechanically isolated from the case 32 which houses all of the othercomponents of the defibrillator, to avoid sensitivity to pressure on thecase. Alternatively, the sensor pair may be housed in its ownbiocompatible hermetically sealed case 38 for implantation in thepatient in a location separate from the defibrillator case, as shown inthe embodiment of FIG. 8.

The lead 40 for connecting the separately housed sensor implant 38 tothe electronic control circuitry of the implanted defibrillator 25 mayhave a proximal end connector of a multiple contact type such as thatdisclosed in U.S. Pat. No. 4,971,057, to facilitate the signalprocessing. The defibrillator case 32 includes a header 43 withelectrical connectors for the lead associated with the activity statussensor implant (if in a separate implantable case) and for the lead(s)connected to the defibrillating and other electrodes for deliveringtherapy and sensing cardiac activity. An ECG sense amplifier and relatedprocessing circuitry included within electronics 29 of the defibrillatorprovide an ECG signal (supplied in raw form from electrode(s) implantedon, in and/or adjacent the heart) for detecting rapid heart rates andother cardiac activity.

In operation, implantable defibrillator 25 is adapted to intervene upondetection of cardiac activity of the implant patient indicative ofpathological VT or of VF by sequentially applying to the heart severaldifferent preprogrammed electrical waveforms conventionally utilized asprotocols for treatment to break the VT or VF, as the case may be, whilemonitoring the patient's cardiac activity from the ECG signal followingthe application of each waveform. If the tachycardia continues or isaccelerating, the protocol may be to successively employ more aggressivetherapies. Therapy is ceased immediately upon detection that thetreatment has been successful.

The activity status sensor detects physical activity and inactivity ofthe patient to complement detection of the patient's cardiac activityfor confirming that a detected VT is a pathological tachycardia ratherthan a physiological tachycardia, if that be the case. Themicroprocessor in the device responds to such confirmation to select anappropriate one of the preprogrammed protocols stored in memory fortreatment, with application of the selected electrical waveform to theheart via the output circuit of the device and the leads. In the exampleof the defibrillator, the shocks intended to defibrillate the heart areproduced by charging the output capacitors of the device to thepredetermined energy level, and then discharging them through the heartin the desired pulse and/or phased waveform, in a conventional manner.

The inability to fully assess the hemodynamic consequences of atachycardia in different patients has frustrated previous attempts toprovide a device universally adaptable to determine whether and when aparticular antitachycardia therapy should be delivered. A particularpatient may be able to tolerate an elevated heart rate of 180 bpm with arapid decline of systolic blood pressure to 65, for example, whileanother patient, because of stenosis and weak cerebral profusion, maysuffer loss of consciousness and respiratory functions with atachycardia rate of 160 bpm and systolic blood pressure of 70.Measurements of heart rate, stroke volume, cardiac output, and evenblood pressure do not fully delineate cerebral status for eachindividual patient. Hemodynamic parameters may appear to be within anormal range or not life-threatening, but they do not provide a trueindication of the cerebral function of the patient.

The problem is exacerbated by the fact that in many individualspathological tachycardia occurs at rates within the high end of the raterange which is normally reached when the patient is engaged in strenuousexercise, such as walking at a brisk pace. Despite the fact that thepatient is ordinarily able to tolerate the elevated heart rate for atleast short periods of exercise, the pathological tachycardia must bebroken because it is not healthy for the heart to beat continuously at arate of, say, 140 or 150 bpm, which is typical of this range, while thepatient is at rest. Further, as noted earlier, the abnormal tachycardiamay accelerate into fibrillation. Therefore, it is imperative that thedevice should provide an appropriate interventional therapy when thissituation occurs, such as stimulation with low energy shocks to breakthe tachycardia.

If a conventional automatic implantable cardioverter and/ordefibrillator were set at a tachycardia recognition rate of 150 bpm, forexample, (and, as noted above, rate alone is the principal criterion,despite these devices using other characteristics of the ECG signal suchas sudden onset or sudden rate change, rate stability, and so forth, asfurther indicia), the implant patient who reaches a heart rate of 152bpm during exercise will be jolted with a stimulation of the heart.Depending on the specific protocol, the inappropriately applied therapymay cause the patient great discomfort and pain, possibly even loss ofconsciousness. If the same patient were to experience pathological VT of140 bpm, therapy would not be applied at that time, and even thoughacceleration past a rate of 150 would then trigger a device response,time is of the essence since the order of difficulty in terminating thetachycardia increases with its longevity and possible progression intoventricular fibrillation. Hence, the patient may suffer very seriousconsequences.

Using an output provided by a non-ECG sensor to additionally indicatewhether the patient is active or inactive when the tachycardia occurs,as in the device and method of the '092 application, helps significantlyto better discriminate between physiological and pathologicaltachycardia. By comparing the ECG signal with the activity statussignal, the occurrence of a slow pathological tachycardia can berecognized by the fact that the elevated heart rate is present withlittle or no physical activity by the patient, as distinguished from aphysiological tachycardia where coincidence of rapid heart rate andpronounced physical activity is evident from the outputs of the twotypes of sensors. Nevertheless, it is not a complete answer because athreshold rate, or tachycardia recognition rate, is still desirable as abasis for comparison.

In the solution provided by the present invention, this threshold rateof the ECG criteria is adjusted according to the output of the non-ECGsensor, which here, as in the '092 application, is preferably anaccelerometer. By observing the processed accelerometer signal, theactivity status of the patient is determined, i.e., inactivity, moderateactivity, strenuous activity, even the position of the patient. Thisinformation is then used to adjust the threshold rate--the tachycardiarecognition criterion of the ECG. In its simplest form, the inventionchanges this rate from a first lower rate to a second higher rate, orvice versa, or simply leaves the existing rate setting in place,according to the status of the output signal of the accelerometer orother non-ECG sensor. In other words, the cardioverter/defibrillator(for example) in which the invention is implemented simply shifts theECG tachycardia recognition rate upward and downward selectivelyaccording to the status of the non-ECG sensor output.

If the accelerometer output signal indicates that the patient is atrest, an appropriate threshold rate (the first lower rate) of 130 bpmmight be selected because it is unlikely (to the point of beingvirtually nil) that emotional stress, fever or other physiological eventthan exercise, which is known to be absent here because of the status ofthe accelerometer output signal, would produce an elevated heart rate ofsuch magnitude. Consequently, anything above this selected (programmed)threshold rate concurrent with such accelerometer output signal isrecognized as a pathological tachycardia. On the other hand, if theaccelerometer output subsequently indicates that the patient isphysically active, the microprocessor of the device shifts the thresholdrate upward to the second higher rate, such as 150 or even 170 bpm, sothe patient may continue to engage in the exercise with consequentincreased heart rate, but without the possibility of being subjected toshocks from the device unless the higher rate is exceeded. Here again,this higher threshold rate is carefully selected to exceed the maximumheart rate that the particular patient in which the device is to beimplanted is likely to have while undergoing strenuous exercise.

In a method for quickly and discriminately recognizing pathologicaltachycardia so that electrical therapy will be delivered promptly to theheart of the cardiac patient to break the tachycardia, the recognitioncriteria provided by the patient's ECG are modified according to thestatus of a non-ECG sensor output signal indicative of the nature andextent of the patient's physical activity or lack of activity. The basiccriterion of heart rate threshold is shifted to higher values withcommencement and any subsequent increases of physical activity, and isshifted back to lower values with decreases and ultimate cessation ofphysical activity.

In a somewhat more complex embodiment and method, the electrical therapyof the implanted medical interventional device is tiered so that ratezones of ECG tachycardia recognition and consequent electrical therapiesare shifted up or down under the control of the output of the non-ECGsensor. Thus, for example, before patient activity commences, thetherapy protocols are bounded at the low end by that therapy associatedwith a recognized tachycardia exceeding the threshold rate for a restoutput signal of the accelerometer. When activity commences, the entirerate zone or range is shifted upward to be bounded at the low end by amoderate threshold rate associated with the low activity output signalof the accelerometer. At that point, the lowest level of therapy (e.g.,least aggressive therapy) for a tachycardia exceeding that moderatethreshold rate is the least available therapy protocol as long as thetachycardia continues. There will be no return to the lower levels oftherapy which were available in the zone having the lowest thresholdrate. The same considerations apply as the activity becomes morestrenuous, and a higher strenuous activity rate is set as the threshold,with the result that treatment will be limited to the still moreaggressive therapies for a pathological tachycardia recognized in thiszone associated with a non-ECG sensor output which indicates a magnitudeindicative of strenuous activity level (exercise workload).

These concepts are illustrated in the graph of FIG. 5, relating heartrate (HR) to time (τ) for a portion of the output signal 50 ofaccelerometer 34 over the time interval of interest. In the period ofpatient rest designated as region 52 of output signal 50, themicroprocessor in electronics system 29 of defibrillator 25 isprogrammed to set the ECG tachycardia recognition rate to 130 bpm. Thus,anything above that relatively low threshold rate (low, owing to thepatient's state of rest) is considered to be a tachycardia for which theelectrical therapy of the device will be administered to the patient'sheart. In region 53 the patient has become active at a moderate activityrate as exhibited by the magnitude of the accelerometer sensor signal,and the microprocessor has responded to this signal by shifting thethreshold rate to 150 bpm in accordance with the programming for thatlevel of the sensor signal. This means, of course, that the patientwould not be subjected to shocking by the device if his heart rate wereto increase to say, 132, because the device has recognized through leveldetection or other conventional means the existence of activity from thenon-ECG sensor output signal necessitating raising the threshold rate.

Subsequently, in region 55 the patient is engaging in more strenuousactivity which results in another ramping up of the threshold rate, to170 bpm in this example. At this point, although the patient's heartrate may be unlikely to reach that level as a consequence of exercise,so too, the margin of safety makes it highly unlikely that he will besubjected to the more aggressive therapy which would be appropriate fora tachycardia rate exceeding 170 bpm, from the exercise alone. Finally,region 56 of the accelerometer output signal indicates that the patienthas returned to a state of resting, and the microprocessor thereforedrops the threshold rate for tachycardia recognition back to 130 bpm.

Tiering of the electrical therapy of defibrillator 25 is accomplished byshifting entire rate zones of the ECG tachycardia recognition and theirrelated electrical therapies upwardly or downwardly based on the outputof the non-ECG sensor. In the graph of FIG. 5, for example, a first ratezone is programmed to exist for the patient at rest, when the output ofthe non-ECG sensor is at or very near zero. In this and every otherzone, the threshold rate is the programmed lower boundary rate of thezone--here, 130 bpm. Thus, in regions 52 and 56 of the time interval ofinterest for output signal 50, a detected ECG heart rate anywhere in thezone above 130 bpm when the output signal of accelerometer 34 reflectspatient resting, is recognized as pathological tachycardia and producesa response under the control of microprocessor 29-1 to deriver a basketof therapy protocols in preprogrammed sequence for as long as thepathological tachycardia remains unbroken. ECG cardiac activity issensed after each therapy is delivered, to assess whether thetachycardia has been broken. As patient activity commences andsubsequently becomes more strenuous, the entire rate zone or range issuccessively shifted upward to be limited by the moderate activitythreshold rate and then the higher strenuous activity threshold rate,and so on. The result is that successively more aggressive therapiesbecome the least available therapies in their respective rate zones asthe output signal of the accelerometer indicates increasing activity bythe patient.

The non-ECG sensor may be any type of known sensor, such as a singleaccelerometer, or two accelerometers as are depicted in FIGS. 2 and 4,indicative of acceleration and hence activity of the patient; a forcesensor indicative for example of movements or pedal impacts and henceactivity of the patient; an impedance sensor for measuring chestimpedance of the patient with ventilation; a blood flow sensor; a bloodpressure sensor; a blood oxygen sensor for measuring oxygen content orsaturation; a blood temperature sensor for measuring changes in centralvenous temperature; a respiration sensor; a minute ventilation sensor;or other sensor characterized by utilization for rate-responsive pacing,including sensors not yet developed, where the parameter being detectedis indicative of or provides additional information on the exercise oractivity status of the patient.

An accelerometer is preferred for the sake of simplicity, rapiddetection and reliability. For example, an accelerometer can be locatedreadily within the device case, as in the preferred embodiment of FIG.4, whereas other types of sensors such as those mentioned abovegenerally require much more elaborate positioning not only outside thecase but in locations requiring special surgical techniques forimplantation in the patient. Further, an accelerometer does not utilizeor require the type of complex technology typically associated with mostother sensors such as those exemplified above, nor have the problems oflong term instability, of drift, of decreased sensitivity in certainstages which characterize these other sensors. Additionally, anaccelerometer is capable of detecting any kind of physical activity, andif two accelerometers are disposed at 90 degrees to one another as inFIG. 2, even the position of the patient may be detected, e.g., whetherhe is lying on his back, lying on his stomach, standing, falling orundergoing some other sudden change in position, and so forth.

FIG. 6 illustrates defibrillator 25 implanted in a patient 60, withlead/electrode assemblies 62, 63 for epicardial patch electrode 65 andan endocardial counter-electrode 71, respectively. The patch electrodeoverlies an appropriate region of the epicardium and thecounter-electrode is positioned in the right ventricle, for efficientdelivery of the high voltage, high energy shock waveform to the heart67. These or associated electrodes may be used to sense and monitor thepatient's ECG and to deliver stimuli (pulses or higher level shocks) tothe heart. Implantable defibrillation apparatus of various types isknown in the art, and the specific type and location of the electrodesis not critical to an understanding of the present invention.

Transvenous lead 63 is preferably of the multi-conductor electrode typeto facilitate and enable detection of signals as well as to deliverelectrical stimulation at multiple locations within the patient's heart.For example, electrode tip 70 is positioned, when the lead is properlyimplanted, to be in direct contact with the myocardium in the rightventricle, and provide ventricular ECG status. Other relatively largesized electrode surfaces 71, 72, 73 and so forth on this lead are usedfor atrial and ventricular cardioversion or defibrillation and forbipolar sensing or conventional bipolar pacing according to devicefunctions and patient requirements at any given time. For example,electrode surface 71 is a coil counter-electrode arranged to bepositioned in the right ventricle for ventricular defibrillation, whileelectrode 73 is of similar configuration adapted to be positioned in ornear the vena cava, when the lead is seated.

Floating electrode points 72 are bipolar electrodes integrated in thelead so as to be positioned in the right atrium when the lead isproperly implanted. The atrial electrodes detect the electrical ECG andmechanical status of the atrium independent of the ventricular signal,so that the status of the atrial chamber is known in relation to thestatus of the ventricular chamber. Such ECG information improves thecapability of the implanted device to discriminate between cardiacevents in the ventricles such as sinus rate, sinus tachycardia,ventricular tachycardia with retrograde block, and others which are ofprimary ventricular origin, from those which are of primary atrialorigin. For example, atrial dysrhythmias such as atrial tachycardia,atrial flutter or atrial fibrillation may be the primary and underlyingcause for a secondary ventricular tachycardia. Accordingly, the ECGsignals obtained from sensing electrodes in the atrium and the ventricleprovide valuable information regarding the origin of a rhythm disorderof interest, and the type of therapy from among the therapies availablefrom the device which are most likely to overcome the disorder andreturn the heart to normal sinus rhythm for the current physiologicalconditions.

Suitable floating electrode signal leads are known from VDD pacingprinciples, and are described, for example, by Brownlee in PACE, vol. 12(March 1989), pp. 431-438, and by Heinz et al. in U.S. Pat. No.5,078,133.

In the implanted device 25, the microprocessor evaluates the informationobtained from the various sensors and applies the selected recognitioncriteria to distinguish between physiological and pathologicaltachycardia, with the interest being in the presence of ventriculartachycardia for reasons mentioned earlier herein. However, it may bethat the VT is secondary, with the primary origin in the atrium. Thisstate of affairs is not evident from the complementary sensor such asthe activity sensor, which, if a pathological tachycardia is present,will simply indicates either that the patient is resting or is engagedin mild physical activity. If this state of affairs were all that isavailable, the device 25 capacitors would be charged and fired todeliver the appropriate cardioverting or defibrillating therapy to theventricles. The result would be an inappropriate firing because suchsecondary VT is attributable to a primary AT here, and the selectedtherapy as well as its point of application would not suffice to breakthe tachycardia.

In this case, however, the microprocessor 29-1 also has the benefit ofthe atrial ECG status information derived from the atrial bipolarelectrode for use in the evaluation, independent of the ventricular ECGstatus. Since this information from the atrium indicates the presence ofAT, the evaluation performed by the microprocessor may be programmed inthose circumstances to attribute the VT to primary atrial origin. Thus,the response is substantially immediate selection by the microprocessorof a therapy regimen to terminate the atrial tachycardia or fibrillationwhich led to the VT. An appropriate therapy, then, where atrialfibrillation is determined by evaluation of the sense signals to be theprimary cause of a secondary VT, is to deliver low energy shocks, suchas in a range from 0.25 to 1.0 joule, from device 25 to the myocardiumof the atrial chambers, via one of the two poles of the bipolar sensingelectrode(s) 72 disposed in the right atrium and the external patch orthe vena cava counter-electrode. A tiered therapy regimen may beemployed here, with the predetermined therapies selected to treat atrialdysrhythmias such as atrial flutter, tachycardia or fibrillation. In anyevent, the selected therapy is strictly or solely a response to anatrial event, such as the application of atrial defibrillation, and toavoid applying high energy shocks to the ventricles.

Moreover, where VT is present when AF is detected, irrespective of theoutput signal derived from the activity sensor (or other non-ECGsensor), it may be, and typically would be desirable to disable furthershifting of the tachycardia recognition criteria, at least until the AFhas been terminated. The reason for this is that the modification ofrecognition criteria is not particularly helpful in these circumstances,and may simply produce undesirable complexities for the analysis.

With reference to FIG. 7, according to a related aspect of theinvention, when a VT is detected the R-R interval, which is the couplinginterval between heartbeats, is monitored by R-R interval detector 80.The purpose is to evaluate the ventricular ECG signals to determinewhether the tachycardia exhibits a regular albeit rapid beat, orundergoes a variation in the R-R intervals. The output signal of the R-Rdetector 80, which representative of this is applied to microprocessor29-1. If an R-R interval variation is occurring, it is an indicationthat an atrial dysrhythmia is present. In that event, the therapy shouldbe applied in a manner to terminate the atrial dysrhythmia. The reasonis that such a therapy will eliminate the VT because the atrial problemis primary, while the VT is only secondary. Here, this is achieved inthe same manner as described above where an atrial dysrhythmia was foundto be primary. The microprocessor controls the capacitors in outputcircuit 82 of device 25 to deliver low energy shocks in the range fromabout 0.25 to about 1.0 joule to the atrial chambers. As before, this isaccomplished through one of the two poles 72 of the bipolar atrialsensing electrode(s) and the patch or counter-electrode. A tieredtherapy regimen may be employed here also.

In contrast, an attempt to terminate such a secondary VT directly, byapplication of high voltage shocks through the ventricles, would proveunsuccessful in addition to causing sever trauma to the patient and amarked reduction in battery life.

When atrial dysrhythmia is found to be the primary cause of the VT, itbecomes undesirable to attempt to modify the tachycardia recognitionrate as was described earlier herein. Such modification of criteria isused for the specific purpose of providing more reliable detection of VTwhen the patient appears to be engaged in exercise. However, when anirregular R-R interval is detected it is clear that exercise is nottaking place. Accordingly, the modification response to the activitysensor output is disabled by the microprocessor when a variation in theR-R interval is detected while a VT is occurring.

Although certain preferred embodiments and methods have been disclosedherein, it will be apparent to those skilled in the art from aconsideration of the foregoing description that variations andmodifications of the described embodiments and methods may be madewithout departing from the true spirit and scope of the invention.Accordingly, it is intended that the invention shall be limited only tothe extent required by the appended claims and the rules and principlesof applicable law.

What is claimed is:
 1. A method for determining which therapy in a tierof electrical therapies is to be applied to the heart of a cardiacpatient to treat pathologic tachycardia, the method including the stepsof establishing different zones for recognizing and distinguishingpathologic tachycardia from physiologic tachycardia, sensing the statusof a physiologic parameter of the patient other than the patient's ECG,shifting the different zones upwardly or downwardly in response to thestatus of said physiologic parameter other than ECG, and correspondinglyshifting the therapies in said tier to be applied to the patient's heartupwardly or downwardly in response to said status, whereby to avoidtreating a detected tachycardia that is purely physiologic with thetherapies.
 2. The method of claim 1, in which the step of sensing thestatus of a physiologic parameter other than ECG is sensing patientactivity.
 3. An implantable medical interventional device for deliveringany of a plurality of different electrical therapies to the heart of animplant patient to treat pathologic tachycardia, comprising:first sensormeans for generating a signal indicative of the patient's cardiacactivity, second sensor means for generating a signal representative ofthe current status of physical activity or lack of physical activity bythe patient, programmable evaluating means for establishing a tier ofsaid plurality of therapies including multiple zones of successivelyhigher threshold rate bounded by respective successively higher upperand lower heart rates to detect a tachycardia from the cardiac activitysignal generated by said first sensor means and to distinguish whetherthe detected tachycardia is pathologic or physiologic in each of saidzones, whereby to avoid treating a detected tachycardia that is purelyphysiologic with said therapies, said programmable evaluating meansincluding comparing means for comparing the rate of the detectedtachycardia to the threshold rate in each of said zones, and controlmeans for shifting upwardly or downwardly through said tier of therapiesin response to sensing respective increases or decreases in the rate ofa pathologic tachycardia in said cardiac activity signal based on thecomparisons with respective threshold rates and on the physical activitystatus signal generated by said second sensor means, so that theparticular one of said therapies within said tier selected to treat thepathologic tachycardia is highly dependent on whether the tachycardia isaccelerating or decelerating.
 4. The device of claim 3, in which:thesecond sensor means comprises a sensor of physical movement.
 5. Thedevice of claim 3, in which:the activity sensor is an accelerometer. 6.The device of claim 5, in which:said control means includes means fordesignating successively more aggressive therapies as the lowesttherapies available in the respective rate zones until the pathologictachycardia is broken.
 7. The device of claim 3, in which:said controlmeans includes means for shifting upwardly or downwardly through saidtier when the signal generated by the second sensor means indicates achange from patient rest to patient exercise, and for shifting theboundary heart rate to a lower rate when the signal generated by thesecond sensor means indicates a change from patient exercise to patientrest.
 8. The device of claim 7, in which:said control means includesmeans for shifting said boundary heart rate to a lower rate comprisingthe original boundary heart rate.
 9. The device of claim 7, in which:thesecond sensor means is an accelerometer.
 10. A method for detectingpathologic tachycardia to determine when to deliver electrical therapyto the heart of a cardiac patient to treat the pathologic tachycardia,comprising the steps of:establishing different zones of heart raterecognition, setting criteria to be applied for evaluating an ECG signalindicative of the patient's cardiac activity to recognize onset andcontinued existence of pathologic tachycardia in the different zones ofheart rate recognition, changing the criteria according to a signalindicating the status of patient activity, the electrical therapy beingtiered according to the different zones of heart rate recognition,applying increasingly aggressive therapies with either continuance oracceleration of the pathologic tachycardia, and shifting the zones ofheart rate recognition, and consequent therapies to be applied, up ordown depending upon the activity signal.
 11. The method of claim 10, inwhich the step of changing the criteria includes determining whether thesignal indicates that patient is resting or active, and if active, theapproximate level of activity.
 12. The method of claim 10, in which thestep of changing the criteria includes shifting a criterionrepresentative of the patient's heart rate among said criteria, saidcriterion indicative of pathologic tachycardia being shifted up or downdepending on whether the activity signal indicates increased ordecreased patient activity, respectively.
 13. The method of claim 10, inwhich the step of changing the criteria includes shifting a criterionrepresentative of the patient's heart rate among said criteria, saidcriterion indicative of pathologic tachycardia being shifted to highervalues with commencement and increases of physical activity by thepatient and to lower values with decreases and cessation of physicalactivity by the patient.